The purpose of these studies is to examine regulation of the cerebral microcirculation 1) during the development of, and following recovery from, experimental hypertensive encephalopathy and 2) by cerebral vasodilator nerves. There are two hypotheses concerning the hemodynamic mechanism of hypertensive encephalopathy: 1) excessive vasoconstriction of cerebral vessels leads to cerebral ischemia and encephalopathy, and 2) passive vasodilation of cerebral vessels exposes the microcirculation of the brain to elevated pressures. Indirect evidence favors the second hypothesis. Using two approaches, I will test the hypothesis that dilation of large cerebral arteries contributes to the pathogenesis of hypertensive encephalopathy in rats. First, I will measure diameter of pial arterioles in rats during the genesis of hypertensive encephalopathy. Second, I will determine whether there is a decrease in resistance of large cerebral arteries during the genesis of hypertensive encephalopathy. The origin of cerebral vasodilator nerves is unclear. I have performed preliminary studies which suggest that the facial and vagal nerves may provide innervation to the internal carotid artery. I will use modern neuroanatomical methods to further examine the origins of the vasodilator nerves. The function of cerebral vasodilator nerves also is uncertain. It has been suggested that vasodilator innervation is greater in large, as opposed to small, cerebral arteries. Thus, the function of cerebral dilator nerves may be to reduce resistance of large, but not small cerebral arteries. I will test the hypothesis that activation of neural cerebrovasodilator pathways, by electrical and chemical means, selectively reduces resistance of large, but not small, cerebral arteries. These studies will provide new information in two areas: 1) the cerebral hemodynamic changes contributing to and following hypertensive encephalopathy, and 2) neural vasodilator regulation of the cerebral circulation, an area in which important basic information is very limited.